C3ar1-flox 基因敲除小鼠

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产品名称

C3ar1-flox 基因敲除小鼠

产品编号

S-CKO-01479

品系全称

C57BL/6JCya-C3ar1em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-12267-C3ar1-B6J-VA

品系状态

使用本品系发表的文献需注明: C3ar1-flox 基因敲除小鼠 mice (Strain S-CKO-01479) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
每周秒杀
cKO小鼠库模型

基本信息

基因研究概述

质控标准

基因
基因全称
complement component 3a receptor 1
基因别称
AZ3B,C3AR,HNFAG09
染色体号
Chr 6 (Mouse)
转录本 ID
NCBI: NM_009779 | Ensembl: ENSMUST00000042081
修饰方式
条件性基因敲除
靶向范围
Exon 2
敲除长度
~1.8 kb
品系说明
该品系是基于策略设计时的数据库信息制作而成,建议您在购买前查询最新的数据库和相关文献,以获取最准确的表型信息。
表型提示
MGI:1097680Homozygous targeted mutants display protective effects against the changes in lung physiology after allergen challenge, increased lethality to endotoxin shock, and elevated IL1B following LPS challenge, supporting the role of C3arin proinflammatory responses.
C3ar1,也称为补体C3a受体1,是一种重要的免疫调节分子。C3ar1属于G蛋白偶联受体家族,能够与补体系统中的C3a配体结合,激活下游的信号通路,从而调节免疫细胞的活化和炎症反应。C3ar1在多种免疫细胞中表达,包括巨噬细胞、树突状细胞、T细胞和B细胞等,参与免疫应答和炎症反应的调节。

C3ar1在多种疾病中发挥重要作用,包括慢性鼻窦炎伴鼻息肉(CRSwNP)、肥胖、非酒精性脂肪性肝炎(NASH)、急性髓系白血病-M2、胃癌和阿尔茨海默病等。在CRSwNP中,C3ar1表达上调,与M2巨噬细胞的浸润和炎症反应相关[1]。在肥胖中,C3ar1表达上调,与VGF基因的表达呈正相关,可能参与肥胖的发生和发展[2]。在NASH中,C3ar1表达上调,与免疫应答和胆固醇代谢相关[3]。在急性髓系白血病-M2中,C3ar1表达上调,与短期生存率相关[4]。在胃癌中,C3ar1表达上调,与不良预后和免疫浸润水平相关[5]。在阿尔茨海默病中,C3ar1表达上调,与tau病理和神经炎症相关[6]。

C3ar1的表达和功能受到多种因素的调节。例如,YAP蛋白可以诱导心脏细胞中的C3ar1表达,参与心脏的再生和修复[7]。此外,C3ar1/C5ar1信号通路的抑制可以导致Foxp3+调节性T细胞(Treg)的稳定性增加,参与免疫调节和炎症反应的调节[8]。此外,C3ar1还可以通过影响STAT3等转录因子的表达,调节免疫细胞的活化和炎症反应[9]。

综上所述,C3ar1是一种重要的免疫调节分子,参与免疫应答和炎症反应的调节。C3ar1在多种疾病中发挥重要作用,包括CRSwNP、肥胖、NASH、急性髓系白血病-M2、胃癌和阿尔茨海默病等。C3ar1的表达和功能受到多种因素的调节,包括YAP蛋白、C3ar1/C5ar1信号通路和转录因子等。C3ar1的研究有助于深入理解免疫调节和炎症反应的机制,为疾病的治疗和预防提供新的思路和策略[1-9]。

参考文献:
1. Zhu, Ying, Sun, Xiwen, Tan, Shaolin, Lin, Hai, Zhang, Weitian. 2022. M2 macrophage-related gene signature in chronic rhinosinusitis with nasal polyps. In Frontiers in immunology, 13, 1047930. doi:10.3389/fimmu.2022.1047930. https://pubmed.ncbi.nlm.nih.gov/36466903/
2. Koc, G, Soyocak, A, Alis, H, Kankaya, B, Kanigur, G. 2020. Changes in VGF and C3aR1 gene expression in human adipose tissue in obesity. In Molecular biology reports, 48, 251-257. doi:10.1007/s11033-020-06043-9. https://pubmed.ncbi.nlm.nih.gov/33306149/
3. Zhang, Jun-Jie, Shen, Yan, Chen, Xiao-Yuan, Zhang, Jie, Xu, Fei. 2023. Integrative network-based analysis on multiple Gene Expression Omnibus datasets identifies novel immune molecular markers implicated in non-alcoholic steatohepatitis. In Frontiers in endocrinology, 14, 1115890. doi:10.3389/fendo.2023.1115890. https://pubmed.ncbi.nlm.nih.gov/37008925/
4. Wu, Shui-Yan, Fan, Junjie, Hong, Dan, Chen, Chien-Shing, Hu, Shao-Yan. 2015. C3aR1 gene overexpressed at initial stage of acute myeloid leukemia-M2 predicting short-term survival. In Leukemia & lymphoma, 56, 2200-2. doi:10.3109/10428194.2014.986481. https://pubmed.ncbi.nlm.nih.gov/25426664/
5. Yang, Haibo, Li, Lin, Liu, Xiaoyu, Zhao, Yu. 2021. High Expression of the Component 3a Receptor 1 (C3AR1) Gene in Stomach Adenocarcinomas Infers a Poor Prognosis and High Immune-Infiltration Levels. In Medical science monitor : international medical journal of experimental and clinical research, 27, e927977. doi:10.12659/MSM.927977. https://pubmed.ncbi.nlm.nih.gov/33539329/
6. Medof, M Edward, Rieder, Sadiye A, Shevach, Ethan M. . Disabled C3ar1/C5ar1 Signaling in Foxp3+ T Regulatory Cells Leads to TSDR Demethylation and Long-Term Stability. In Journal of immunology (Baltimore, Md. : 1950), 211, 1359-1366. doi:10.4049/jimmunol.2300184. https://pubmed.ncbi.nlm.nih.gov/37756526/
7. Li, Rich Gang, Li, Xiao, Morikawa, Yuka, Samee, Md Abul Hassan, Martin, James F. 2024. YAP induces a neonatal-like pro-renewal niche in the adult heart. In Nature cardiovascular research, 3, 283-300. doi:10.1038/s44161-024-00428-w. https://pubmed.ncbi.nlm.nih.gov/38510108/
8. Abdolmaleky, Hamid Mostafavi, Zhou, Jin-Rong. 2023. Underlying Mechanisms of Brain Aging and Neurodegenerative Diseases as Potential Targets for Preventive or Therapeutic Strategies Using Phytochemicals. In Nutrients, 15, . doi:10.3390/nu15153456. https://pubmed.ncbi.nlm.nih.gov/37571393/
9. Litvinchuk, Alexandra, Wan, Ying-Wooi, Swartzlander, Dan B, Liu, Zhandong, Zheng, Hui. 2018. Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer's Disease. In Neuron, 100, 1337-1353.e5. doi:10.1016/j.neuron.2018.10.031. https://pubmed.ncbi.nlm.nih.gov/30415998/